PML - The clinical diagnosis of PML is confirmed
by histological and virological examination of brain
material obtained by brain biopsy or at postmortem.
Before a biopsy is done, both serum and CSF should be
examined for antibodies against JCV. A positive result
will not confirm PML, but a negative result makes the
diagnosis of PML very unlikely. It is rare to detect
antibodies against JC in the CSF. When it is detected, it
is suggestive of active multiplication of JCV within the
CNS. The brain biopsy or autopsy material can be examined
by EM or IEM. The specimen can also be examined directly
for JCV antigen by immunofluorescence or immunoperoxidase
staining. Virus isolation is very difficult for JCV. When
attempted, primary human fetal glial cells are used. The
presence of the virus in culture is confirmed by EM, IF
or haemagglutination. JC is rarely excreted in the urine
of patients suffering form PML.
Renal Tract Infections - the methods generally
employed to detect the presence of polyomavirus in urine
are cytological examination of the urine for
inclusion-bearing cells, EM and virus isolation. The
cytology of urine in human polyomavirus infection is
quite characteristic. The inclusion-bearing cells have a
characteristic appearance and are often present in large
numbers. Electron Microscopy of the urinary sediment
after centrifugation at 20000 may reveal the presence of
polyomavirus particles. It is difficult to isolate JC and
BK viruses: Primary PHFG cells must be used for isolation
of JCV; BKV have a wider host cell range and HEK cells
can be used as well as PHFG cells. More sensitive
techniques are being developed, such as dot- blot and
Serological Diagnosis - HAI is the most widely
used serological technique for measuring antibodies
against the polyomaviruses. CFT, neutralization, ELISA
and RIAs have also been used.
Because of the invariably fatal outcome of PML, various
antiviral drugs have been tried. The only drug that may have had
an effect is cytarabine. Reports have been published on 8
laboratory confirmed cases of PML treated with cytarabine.
Long-term improvement was seen in 2 patients. In another person,
there was a dramatic response to therapy within 24 hours but this
was not maintained. The rapid progression of the disease was
halted in a fourth patient but the neurological damage was
severe. The remaining 4 individuals did not show any improvement.
One should also consider relaxing any immunosuppression regimes
in such patients.